12
5966
[JAN. 1, 1938
ADDRESSES AND ORIGINAL ARTICLES
SURGICAL TREATMENT OF ANGINA
PECTORIS
AND ALLIED CONDITIONS
BY DANIEL T. DAVIES, M.D.Wales, F.R.C.P.Lond.
H. E. MANSELL, B.M. Oxon., F.R.C.P. Lond.AND
LAURENCE O’SHAUGHNESSY, F.R.C.S. Eng.
With the coöperation ofVISCOUNT DAWSON OF PENN, P.C., M.D., B.Sc.,
P.R.C.P. Lond.
(From the Cardiovascular Clinic, Lambeth Hospital,London County Council)
THE experimental basis and technique of cardio-omentopexy was described a year ago in a speciallecture at the Royal College of Surgeons of Englandwhich was introduced by Lord Dawson of Penn,honorary consultant to the Lambeth CardiovascularClinic, and published in this journal. The presentpaper contains an account of the further experiencesof the clinic with cardio-omentopexy and othersurgical means of supplementing a deficient coronarycirculation.
In the Registrar-General’s report for 1935 12,317deaths are recorded from angina pectoris and coronarydisease, and it seems probable that cardiac ischsemiaplayed an important part in at least some of theenormous total of 70,504 deaths from myocardialdisease. The total figure for carcinoma is 66,000.The relation of coronary disease to sudden deathhas long been realised. Leyden, writing in the
eighties, recognised the clear relation between degen-erative changes in the myocardium and sclerosis ofthe coronary tree. Huchard agreed with Leyden,but by 1915 Sir Clifford Allbutt, while not denyingthe occasional existence of gross coronary obstructionas a cause of death, regarded angina as a symptomnot of cardiac isch2emia but of some undefined typeof nervous degeneration in the aortic plexus. To-dayby common consent opinion has returned to the olderview. On the clinical side Levine, in his clear andconcise monograph, has grouped under the generalheading of Angina Pectoris all the organic causes
of cardiac ischaemia—coronary thrombosis, coronarysclerosis, and syphilitic aortitis-and he is emphaticthat in fatal angina structural change is alwayspresent both in the myocardium and in the coronarytree. It is gradually being recognised that " chronicmyocarditis " is a comparatively rare disease apartfrom cases of syphilitic or rheumatic origin, and thatthe greater proportion of cases so labelled, if carefullyexamined post mortem, show evidence of coronarydisease.
Biichner, Weber, and Haager (1935) have publisheda careful record of 43 fatal cases of cardiac ischæmiain which the clinical findings are correlated with thepost-mortem appearances both macroscopic andmicroscopic. They describe coronary thrombosis inan otherwise normal coronary tree, thrombosis com-plicating atheroma of the coronary arteries, hyper-tensive heart failure with gross atheroma of the treebut no gross obstruction, and syphilitic aortitis inwhich only the orifices of the vessels were affected.In every case the electrocardiograms were charac-
teristic of cardiac ischaemia, and at autopsy carefulexamination of the heart revealed pathologicalchanges in the myocardium. After obstruction of amain vessel, gross evidence of an old or recent infarctwas invariably present ; and where no actual blockof the circuit was found but merely a general impair-ment of its lumen, scattered areas of recent necrosisor old fibrosis could always be detected in serialsections.Under some conditions coronary occlusion is a
fatal event, but the organism is often in a positionto effect a remarkable degree of compensation ; evensuccessive attacks of coronary thrombosis may besurvived and an astonishing degree of normal activitymay be regained in the interval, sometimes years inextent, between the initial and the second attack.The mechanisms by which this natural compensationmay be brought about have already been consideredin previous papers. Although it is quite possible thatthere may be some subtle mechanism of which weknow nothing, there are only two methods for theefficacy of which we have experimental and clinicalevidence. One of these is anastomosis between theright and left coronary arteries, and the other is theprocess by which the heart may supplement its blood-supply from the parietes. The first mechanism isclearly of no avail when a diffuse sclerosis affects theentire coronary tree, and the second is only availableif partial or complete destruction of the epicardiumtakes place so that adhesions may form between theheart and the parietal pericardium. After a coronarythrombosis only a small proportion of patients formadhesions between their infarct and the parietal peri-cardium, but this mode of compensation is importantbecause it alone can be initiated or supplemented bysurgery.
In a previous paper examples of the beneficialassociation of pericarditis with coronary disease werereviewed-Sternberg’s classical case of " pericarditisepistenocardica," the histories cited by Monckeberg,and also Sir Clifford Allbutt’s doctor patient whoreturned to active practice after a severe attack ofangina complicated by pericarditis. Chance hasprovided us with an excellent example of naturalcompensation in angina pectoris.The father of one of our operated patients is now
aged 68. For several years he suffered from anginafor which he received the usual medical treatment. Threeyears ago he was suddenly seized by a more violent attackof pain in his chest than he had previously experienced,and in a state of collapse he was removed to hospital,where he passed some days in a critical state and gravedoubts of his ultimate recovery were expressed. How-ever, he recovered and after some weeks in bed returnedhome. He gradually resumed general activity and wasamazed to find that his angina had disappeared. Heremains free from pain and our interpretation of hisrecovery is that he suffered an attack of coronarythrombosis and adhesions formed with the parietes.
Moritz demonstrated by injection studies thevascularity of pericardial adhesions, and similarresults have been obtained by one of us (H. E. M.) inthe pathological department at Lambeth. In casesof pericarditis following coronary thrombosis it waspossible to demonstrate vascular continuity betweenthe coronary tree and the vessels of the parietal peri-cardium, the inferior sternopericardial ligament, andthe diaphragm. It may be mentioned that thevascularity of the structures surrounding the heartin human beings appears to be much greater than inexperimental animals.
A
2
A review of the literature of coronary disease showsthat methods of initiating or supplementing thecollateral blood-supply to the heart are engaging theattention of physicians both in America and inGermany. Hochrein in his latest monograph (1937)states that " we have learnt to recognise that peri-
FIG. 1.—Section through junction between myocardium (above)and omentum (below) a week after operation. A primitivevessel is growing from the omentum into the heart muscle.(x 60.)
carditis is not a complication of coronary thrombosisbut a natural attempt at healing-its presence is tobe welcomed rather than deplored," and he goes onto discuss the theoretical possibility of encouragingthe formation of pericardial adhesions when naturehas failed to provide them. This theoretical possi-bility has been carried into practice in some of ourcases with apparently beneficial results.
Experimental Basis of Cardio-omentopexy andAllied Operations
Experimental work on various methods of aug-menting the blood-supply to the heart has been inprogress at the Buckston Browne farm of the RoyalCollege of Surgeons of England since April, 1933.The results previously obtained have been recordedin various publications, and a further paper con-taining details of modifications in technique is in
preparation.In animal experiments we have shown that an
omental graft attached to the heart is compatiblewith the highest degree of physical exertion. Oneof our greyhounds completed a full course (525 yards)without distress after his recovery from two opera-tions-at the first the descending branch of the leftcoronary artery was tied and at the second the graftwas applied.We have also shown that vascular connexions
rapidly form between the graft and the myocardium,whether it is attached to normal muscle, to the siteof a recent infarct, or to the site of an old fibrousinfarct ; this is important because these are the threeconditions with which one might be confronted atoperation. New vessels may be observed micro-
scopically at the end of a week (Fig. 1), and at theend of three weeks complete injection of the coronarytree may be carried out from the graft with a sus-pension of indian ink. As time passes the vascularconnexion increases and these injections may bemade with barium paste (Fig. 2). The oldest speci-men examined-that of a greyhound killed eighteenmonths after operation-showed that there was amarked increase in the normal mediastinal vessels
and that these too had made connexions with thegraft and with the myocardium. It is a fundamentalpoint that cardio-omentopexy brings a new blood-supply to the heart from the abdominal aorta andalso supplements the normal collaterals in the medi-astinum and gives them access to the ischsemic heart.It is also important to realise that the graft formsdirect connexions with the myocardium at its pointof attachment and that its vessels anastomose withbranches of the coronary tree, and therefore bloodbrought by the graft may be distributed to all partsof the heart. In other words, exact placing of thegraft in relation to any localised area of ischgemiawhich it is desired to influence is not essential.
Lezius (1937) has shown that the lung can formextensive vascular adhesions with the heart whenthe fibrous pericardium is removed ; he found thatunder these conditions he could ligature the descend-ing branch of the left coronary artery without causingthe usual infarct. In cardio-omentopexy the lungoften adheres to the graft and probably assistsin revascularisation, but we have so far only usedcardio-pneumonopexy when the usual operation wasimpossible.
In the most recent of our laboratory experiments wehave shown that the production of intrapericardialadhesions by the use of a special preparation-Aleuronat-provided us with an additional and simplemeans of revascularisation. In this way a route isafforded for revascularisation from the mediastinalvessels, but the method is inferior to cardio-omento-pexy in that reinforcement of these vessels does notoccur.
In our earlier experiments and operations theomental graft was always sutured to the heart; morerecently we have been able to obtain equally firmattachment of the graft by suturing it to the peri-cardium only and applying aleuronat paste betweenthe graft and the heart. We have also been able todemonstrate that the vascular continuity under theseconditions is of the same order as when sutures areemployed. This is technically important, for ourexperience has shown the danger of placing suturesin a friable and degenerate heart.
The OperationsFour types of operation were used in this series :Cardio-omentopexy (Fig. 3) in which a left trans-
pleural exposure of the heart is used, the pericardiumis opened and a pedicled graft of the great omentumis brought through the diaphragm and attached tothe heart.
Transpleural pericardiotomy in which the peri-cardium is opened after a left transpleural exposure,aleuronat paste is inserted and the pericardium isclosed.
Extrapleural pericardiotomy in which the seventhcostal cartilage and part of the xiphoid process areresected in Larrey’s angle, the pericardium is openedand the sac treated with aleuronat.
Cardio-pneumonopexy (Lezius) in which after a lefttranspleural approach the pericardium is opened anda portion of lung is attached to the heart.
The Cases
The series consists of twenty cases. Patients wereselected for operation who showed unequivocalevidence of cardiac ischaemia and who had failed tobenefit by medical treatment. The majority weresuffering from angina of effort. The aim of the
operation in every case was to supplement the
3
coronary circulation from without. The actual tech-
nique was modified to suit the individual patient andvaried from complete cardio-omentopexy to simplepericardiotomy for insertion of the irritant aleuronatto encourage pericardial adhesions.The cases will be considered in two groups-the
first and larger group consisting of patients sufferingfrom angina pectoris, the second and smaller groupconsisting of patients with other symptoms of cardiacisch2amia.
GROUP I: ANGINA PECTORIS
Of the fifteen members of this group (Table I)some were bedridden, others were in hospital, and therest with one exception suffered from angina of effortof such degree as to curtial their ordinary activity.The exception is Case 13, in which the pain was notsevere and was due to his previous coronary throm-bosis, but in view of his age we considered operationjustifiable.
CASE 1
A cosmopolitan of varying occupations, aged 65, wastransferred to Lambeth Hospital on July 28th, 1936,from St. Stephen’s Hospital (L.C.C.), where he had beenadmitted on July 7th after an attack of severe angina onthe previous day. The pain had been most severe,lasting for four hours without relief from amyl nitrite andaccompanied by much dyspnoea. He had had eightattacks during the previous four years, and from thefirst attack had limited his activities as far as possible.He was not normally breathless on exertion. He had hadsevere insomnia for the past six or eight months. Hewas a heavy smoker until three years ago. He gave ahistory of malaria and three laparotomies-for appendi-citis, adhesions, and gastro-enterostomy. A paternaluncle had " dropped dead of angina."
Physical examination showed a grey-haired, well-nourished man with somewhat protruding eyes. Histongue was clean. There was no enlargement of thethyroid but slight tremor of the fingers. The radialartery was slightly tortuous but not thickened. The heartwas not enlarged, the sounds were normal, and there wasa soft apical systolic murmur. The blood pressure was
A . B
FIG. 2a.-Greyhound’s heart injected with barium paste through the graft, eighteenmonths after cardio-omentopexy. Left side with graft attached.
FIG 2b-Right side of the same heart.
116 mm. systolic and 72 diastolic. The lungs were
emphysematous. The abdomen showed three well-healedscars. The right pupil was larger than the left and theknee-jerks and ankle-jerks were not elicited. The urinewas normal and the blood-urea 32 mg. per 100 c.cm.
The Wassermann reaction was negative. X ray examina-tion showed a
large heartshadow. Thebasal meta-bolic rate was- 40 per cent.The electrocar-
diogram showedthe S-T inter-val raised andconvex down-wards in leadsII and III.
Cardio - omen-topexy was per-formed onAugust 17th.The heart wasfound to be freeof pericardialadhesions.There was no
difficulty in
obtaining omen-tum in spite ofthree previous
FIG. 3.-Diagram illustrating cardio-omentopexy in man.
laparotomies. At the end of operation the upperleft intercostal nerves were injected with 1 per cent.novocain. The pulse-rate was 96. Except for, animmediate mild bronchitis recovery was uneventful. Hewas allowed up four weeks later and took his own dis-charge on Dec. 10th, the blood pressure being 160 mm.systolic and 90 diastolic. There were no further attacksof angina. Movement of the left diaphragm was seenfor the first time 3 months after operation. Serialelectrocardiograms showed a gradual emergence of a
Q wave in lead III.Since leaving hospital he has been able to lead a life of
normal activity without symptoms.
CASE 2
A male, aged 71, who had retiredfrom the Burma Police thirty yearspreviously, was admitted to LambethHospital from Dr. Dean Pollard ofBedford on July 31st, 1936, complain-ing of attacks of pain, beginning atthe base of the neck and spreadingover the heart and down the left arm.The first attack had occurred sud-denly during exertion three yearspreviously. They had become in-
creasingly frequent-now almost daily-but not more severe. The pain wasalways related to exertion, emotionor, during sleep, to nightmare, andwas relieved by nitroglycerin. Hewas not breathless on exertion be-tween the attacks. He gave a historyof appendicectomy in 1912.
Physical examination showed a well-nourished man of rather plethoricfacies. His remaining teeth were
septic. The radial arteries were
tortuous and thickened. The size ofthe heart was masked by emphy-sema. The sounds were very distantbut not spaced, and there was a softsystolic murmur at the apex. Theblood pressure was 205 mm. systolicand 105 diastolic. Nothing abnormalwas found in the lungs, abdomen, andcentral nervous system. The urinewas normal and the blood-urea 44 mg.per 100 c.cm. The Wassermann
4 DR. DANIEL DAVIES AND OTHERS : SURGICAL TREATMENT OF ANGINA PECTORIS
TABLE I-CASES OF ANGINA PECTORIS
reaction was negative. X ray examination showed thatthe heart was not enlarged. The electrocardiogramshowed left axis-deviation, with inversion of the T wavesin lead I. The S-T interval was depressed in lead I andraised in lead III.While in hospital he had two attacks of angina : a
mild attack in our presence while walking too fast, and asevere attack lasting six or seven minutes while strainingat stool. On August 17th he developed acute tonsillitisand was sent home to recuperate on the 26th. He wasreadmitted on Sept. 23rd ; he had a severe attack lastingtwenty minutes on the station, after climbing a flight of24 steps twice, and had to take two tablets of nitro-
glycerin before being able to proceed. On examinationhe looked fit and the throat was clear. The blood pressurewas 208 mm. systolic and 118 diastolic. There were nobasal rales and the urine was normal. The electro-
cardiogram showed no change.Cardio-omentopexy was performed on Sept. 25th. The
pericardium was tense, and the heart enlarged but freeof adhesions. The pulse-rate at the end of operation was72, and the blood pressure two hours later was 154 mm.systolic and 92 diastolic. The electrocardiogram showedno change.He developed purulent bronchitis which lasted a week.
On Oct. 4th he had two attacks of angina following visitinghours, the second needing an injection of morphia. Therewas a slight attack two days later. On Oct. 12th he hada severe attack (after being allowed up for two hours bymistake), only partially relieved by nitroglycerin andmorphia and leaving numbness of the left arm. Hesubsequently became subject to frequent attacks of pain,occurring day and night and not related to exertion.The pain was relieved by nitroglycerin but not by aninjection of sterile water. Attacks did not occur when hisattention was occupied. He began to get up at the endof four weeks and was discharged home on Nov. 1st,showing no ill effects from a long car journey. His wifewrote on Nov. 30th : " He is immensely improved bothmentally and physically, and I think that he improvesslowly all the time. If it were not for occasional
pains, he would be in perfect health." During the
following week there was a return of severe pain andinsomnia. The pain soon eased off, to be followed bybreathlessness which became more and more distressing
until Dec. 19th, when he was readmitted to LambethHospital.On examination he looked haggard and desperately ill.
There was Cheyne-Stokes breathing, but in spite of theviolence of the hyperpnoeio phase he had no angina. The
pulse was of fair volume and rate 100. The heart soundswere of very poor quality and there was gallop rhythm.The blood pressure was 140 mm. systolic and 100 diastolic.Rales were audible at the left base. There was no oedemabut the urine was loaded with albumin. The tongue wasdry and coated. The electrocardiogram showed muchincrease in voltage of the S waves in lead III and changes
FIG. 4.-Section from Case 2 through junction between myo-cardium and omentum three months after operation. Avessel is seen entering the myocardium.
in the S-T interval in leads I and III. A diagnosis ofuraemia was made. The blood-urea proved to be 116 mg.per 100 c.cm. and the blood calcium 10.4 mg. He improved
5DR. DANIEL DAVIES AND OTHERS : SURGICAL TREATMENT OF ANGINA PECTORIS
for a few days with treatment but changed suddenly forthe worse on Dec. 27th and died that night.
Post-mortem examination showed the operation woundto be firmly healed and there had been complete restitutionof the thoracic cage. The graft was firmly attached tothe heart, which was removed for injection. The rightpleural cavity contained free fluid in excess but the lungwas normal. The lower lobe of the left lung was collapsed.The abdomen contained an excess of free fluid, but theviscera, including the colon, were normal, and the graftcould be seen in place passing through the diaphragm.The kidneys showed chronic interstitial nephritis andthere was advanced atheromaof the abdominal aorta. Injec-tion of the graft with a waterysuspension of indian ink wascarried out from the abdominalaorta, after removal from the
body. A pressure of 100 mm.of mercury was used, and thetechnique was identical withthat employed in the experi-mental series. A very profuseinjection of the parietal peri-cardium was obtained, and theink eventually reached thechambers of the heart. Thespecimen was fixed in formalin,and on section it was possibleto see ink lying in the myo-cardium. Stained sectionsshowed new vessels runningfrom the omentum into the
myocardium (Fig. 4). Therewas diffuse sclerosis of the
coronary tree, the lumen beingobliterated at one point on theleft descending branch, butthere was no actual infarctionof the myocardium.
CASE 4
A missionary’s widow, aged65, was admitted to LambethHospital from Dr. Lyne ofHove on Oct. 1st, 1936, with ahistory of angina of twelve
years’ duration. It had for-
merly been relieved by amylnitrite but now needed Omno-
pon. Attacks were often occur-
ring at night, or in the earlymorning if she had becomeovertired the evening before.She had been practically con-fined to bed for eighteen monthspast and was unable now towash herself. She was alsoliable to attacks of rapid andirregular pulse, lasting about half an hour and causingconsiderable distress at the time. She also complainedof headache and a bursting feeling in the head. She hadled an exceptionally adventurous and strenuous life,often at high altitudes. She had had pleurisy severaltimes, and pneumonia eight years ago. There is a familyhistory of pulmonary tuberculosis. A sister died of astroke and another has angina.On examination she was obese. The teeth were well
stopped, the throat clear. The apex-beat was in the5th intercostal space in the anterior axillary line. Themitral first sound was very low and the aortic secondsound accentuated and ringing. There was a very softto-and-fro murmur at the apex and in the aortic area.The blood pressure was 247 mm. systolic and 117 diastolic.Nothing abnormal was found in the chest and abdomen.The knee-jerks and ankle-jerks were not obtained. Therewas no oedema and the urine was normal. TheWassermann reaction was negative. X ray examina-tion showed a large heart. The electrocardiogram showeda right (old terminology) bundle-branch block, with verylarge amplitude of the Q R S complexes in leads I and III.
(The bundle block was known to have been present in1930.) She was treated for fourteen days with a starch-free diet, general massage, and sedative drugs.
Cardio-omentopexy was performed on Oct. 16th. Theinferior sternopericardial ligament was fatty and wellmarked. A large fatty graft was secured and sutured tothe heart, which was free of adhesions, aleuronat in addi-tion being inserted. At the end of operation the pulse-rate was 69 and the blood pressure 170 mm. systolic and90 diastolic. Recovery was interrupted by a paroxysmof auricular fibrillation, which began 30 hours afterwardsand ceased spontaneously 9i hours later. It was accom-
FIG. 5.-Serial electrocardiograms taken in Case 5. Cardio-omentopexy with insertionof aleuronat was performed on Jan. 22nd.
panied at the onset by severe angina. There was a moderaterise of evening temperature for four days. Two anginalattacks occurred in the first fortnight and none sub-sequently. General massage was restarted after five weeksand she was allowed to wash herself. In six weeks theblood pressure had returned to 240 mm. systolic and112 diastolic. On Christmas Day, ten weeks after opera-tion, she was up and about the ward for two hours withoutill effects. During January she had some further attacksof paroxysmal fibrillation accompanied by pain. Theyceased as soon as she was put on quinidine. She wastransferred to St. Benedict’s Hospital for convalescenceon Feb. 3rd, sixteen weeks after operation. The bloodpressure was 230 mm. systolic and 116 diastolic; theelectrocardiogram showed no change and there were
still signs of collapse at the left base.She was discharged from St. Benedict’s Hospital on
March 18th and has gradually regained her activity.There have been no more attacks of angina. There wasa brief return of auricular fibrillation in June when shehad been overdoing things, but it responded at once toquinidine. Eight months after operation X ray examination
6
showed the left diaphragm moving synchronously withthe right, and there were no longer signs of collapseat the left base. She is now leading a life of activitynormal for her age without any pain.
CASE 5
An engineer, aged 60, was admitted to Lambeth Hospitalon Jan. 12th, 1937, with a four years’ history of anginapectoris. Attacks had gradually increased in frequencyand during the past few months had made his life unbear-able. They had occurred occasionally in bed. Pain wasrelieved by nitroglycerin. He had led a very active life,chiefly in the tropics for the last thirty years. He was astrong man, well known for weight-lifting and wrestling,a big spirit-drinker and heavy smoker. There was nofamily history of angina.
Physical examination showed a well-developed man ofheight 5 ft. 8i in. and weight 13i st. There was noevident arterio-sclerosis. The heart was not enlarged, themitral first sound was accentuated and low-pitched, theaortic second sound clear, and there were no murmurs.Nothing abnormal was found in the chest, abdomen, andcentral nervous system. There was a small left inguinalhernia. The urine was normal and the blood-urea 32 mg.per 100 c.cm. The Wassermann reaction was negative.X ray examination showed no enlargement of the heart.The electrocardiogram showed left axis-deviation andlow T waves in lead I.
Cardio-omentopexy was performed on Jan. 22nd. Theomentum was easily obtained, but some difficulty wasmet in getting enough without bringing the stomach withit. The heart was not enlarged and was free of adhesions.Aleuronat was applied and the graft was sutured to theheart and pericardium. The pulse-rate at the end of
operation was 108 and the blood pressure 140 mm. systolicand 85 diastolic. He developed mild purulent bronchitisand fever lasting a fortnight. During the first week hehad several paroxysms of auricular fibrillation, but thesewere readily controlled by quinidine. During the secondweek he developed signs and X ray evidence of a smallleft pleural effusion. At the end of a fortnight he had anattack of angina, and in less than a month he was gettingattacks as often as before the operation. They wererelieved by nitroglycerin. He was allowed up at the endof four weeks, and was transferred to Sidcup for con-valescence on March 30th, his blood pressure being 156 mm.systolic and 96 diastolic. Serial electrocardiograms (Fig. 5)showed inversion of the T waves in leads I, II, and IV,most marked between the fourth and sixth weeks after
operation.Attacks of pain became gradually less frequent and the
consumption of nitroglycerin tablets less, but, it was sevenmonths before he reported himself symptom-free. Before
operation five stairs were all he could manage. He nowclimbs sixty to his room without pain or distress. InNovember he successfully underwent radical herniotomyunder general anaesthesia.
CASE 7
A widow, aged 67, was admitted to Lambeth Hospitalon Feb. 5th, 1937, at her own request, complaining ofangina pectoris of two years’ duration. The attacks werefrequent and severe, and she could not even put on hershoes without inducing pain. Nitroglycerin gave hershort-lived relief. Against her family’s wishes she desiredoperation, even if it were to prove fatal. Ten years agoshe had been treated in Bethnal Green Hospital for hyper-tension. Two years ago she had a stroke with left
hemiplegia. There was a history of pleurisy as a youngwoman. Her mother died of " aneurysm of the heart."
Physical examination showed a well-nourished, grey-haired woman. The brachial arteries were full and elastic.The apex-beat was in the 5th intercostal space, 4i in. out.The cardiac impulse was heaving. The mitral first soundwas low-pitched and the sounds rather spaced. A
systolic murmur was audible in all areas and maximalin the pulmonary area. The blood pressure was 200 mm.systolic and 118 diastolic. There were rales at the bases.The abdomen was normal. The right pupil was smallerthan the left and did not react, and the ankle-jerks werenot obtained. There was very slight oedema over the
tibise. The urine and kidney function tests were normaland the blood-urea 36 ing. per 100 c.cm. The Wassermannreaction was negative. X ray examination showed theright diaphragm raised but moving normally. The heartwas not enlarged. The electrocardiogram showed well-marked Q waves and flat T waves in lead III. Operationwas postponed for a week owing to slight coryza but wasthen undertaken at her urgent request.
Thoracotomy was performed on Feb. 26th and the
phrenic nerve crushed. A good graft was secured andthe edge of it was sutured to a well-marked and vascularsternopericardial ligament. The pericardium was openedeasily, there being no tension and no adhesions. Theanterior descending branch of the left coronary was muchmore exposed than usual and was tortuous but notcalcified. The first myocardial suture was inserted to theright of this vessel without incident, although a clearview of the myocardium was obscured by subepicardialfat. A second suture was inserted and immediatelybleeding was observed. The suture was at once tied, withthe result that much more violent haemorrhage occurred.It now become obvious that the wall of the right ventriclehad been torn, and the bleeding point was seized with aMoynihan forceps, which tore through, leaving a largegaping wound in the ventricular wall. Three fingers of theoperator’s left hand were inserted into the defect so thathaemorrhage was controlled. Chordae tendinese were
clearly felt in the ventricular cavity. One assistant thenenlarged the intercostal incision, while the other openedthe pericardium widely. The heart was now completelydelivered from the wound, and while venous return wascontrolled by manual compression of the cavae the largerent was repaired by interrupted sutures, supplementedby free muscle graft ; and in addition a smaller rent onthe posterior wall of the right ventricle was repairedin a similar manner. The heart was returned, the cavsereleased, and at once a small tear was apparent in the wallof the right auricle. The heart was again delivered,the cavse again controlled, and this tear repaired. Theheart was replaced and was seen to fill with blood withouthaemorrhage. During the whole manceuvre the totalamount of blood lost was small, and the auricles wereobserved to be contracting again rhythmically. Cardiacmassage and intracardiac adrenaline failed to restoreventricular action. The estimated duration of caval
compression was 3i and li minutes.At post-mortem examination the brain showed an area
of old softening in the upper aspect of the posterior part ofthe right frontal lobe, and there was severe atheromaof the cerebral arteries. The heart weighed 10 oz., andthe myocardium very friable. There were two tears inthe ventricular wall, both sutured and one also pluggedwith a portion of voluntary muscle, and there was asubpericardial haematoma over the left auricle close to a.sutured rent in the coronary sinus. Severe coronaryatheroma was present. There was considerable atheromaof the lower abdominal aorta. The lungs were congestedand showed basal collapse, especially on the left side.The kidneys and their vessels appeared normal.
CASE 8
A machine-hand, aged 56, was admitted to LambethHospital from Dr. W. G. Watson on Feb. 20th, 1937,complaining of shortness of breath for eighteen months andpain over the heart, on exertion only, for six months.The pain lasted about two minutes and radiated into theleft arm ; it was never agonising, had never occurred atrest, and was more likely to occur after a heavy meal.There were no other symptoms. There were no previousillnesses and he was passed Al in the war. There was no
history of angina in the family.Physical examination showed a well-nourished man with
a high colour. The tongue was moist and clean and histeeth had all been extracted about three years beforefor neuralgia. The heart was not enlarged, the aorticsecond sound was thin and sharp, and there was a systolicmurmur at the apex. Frequent extrasystoles were present.There was moderate radial and brachial arterio-sclerosis,and the blood pressure was 150-130 mm. systolic and75 diastolic. Nothing abnormal was found in the abdomenand central nervous system. There was very slight
7
pitting over the left tibia. The urine and kidney functiontests were normal and the blood-urea 28 mg. per 100 c.cm.’The Wassermann reaction was negative. X ray examina-tion showed a long thorax, with nothing abnormal inthe heart, lungs, or aorta. The electrocardiogram showedsome slurring of S in all leads and numerous prematureventricular contractions. He was diagnosed as an earlycase of angina pectoris.
Operation was performed on March 5th, the pericardiumbeing opened via Larrey’s angle and aleuronat being
FIG. 6.-Temperature chart showing aleuronat reaction.
- inserted. There was pyrexia (Fig. 6) for eleven days andthe extrasystoles became more numerous. A soft peri-cardial rub was heard and X ray examination suggesteda small pericardial effusion. He was allowed up afterthree weeks and discharged home on April 6th. He hadhad no pain since the operation but extrasystoles werestill present. The electrocardiogram showed marked,elevation of the S-T interval, especially in lead II, duringthe first week, and this was followed at the end of threeweeks by flattening or inversion of the T waves in all leads.’Three months after operation the T waves had returned tomormal in leads I and II but remained inverted in lead III.
There has been no pain since operation. He complainedof some breathlessness on exertion for the first three monthsbut is now symptom-free and back at work.
CASE 9
A secretary, aged 50, was admitted to Lambeth Hospitalon March 7th with a history of anginal attacks for fouryears. Two attacks had been particularly severe : one
- eighteen months before, when the pain had occurred atrest and lasted 48 hours and he was in bed for three weeks ;and the other four weeks before admission, when the painagain came on during rest, lasted 24 hours, and he was inbed for two days. An attack was " always hanging,about," and his activity was greatly curtailed. Amylnitrite had given some relief. He had been compelled tomove into a bungalow to avoid stairs and had given up- driving a car. His previous history was negative, exceptfor influenza in 1918. His father had one stroke beforehe died of chest trouble, and his mother died of a stroke.A maternal uncle died suddenly of a severe pain in the- chest.
Physical examination showed an obese man, 5 ft. 4i in.in height and weighing 12 st. 4 lb. The heart was not- enlarged, the sounds were normal, and there were nomurmurs. The blood pressure was 140 mm. systolic and100 diastolic, and there was no arterio-sclerosis. Nothingabnormal was found in the chest, abdomen, and centralnervous system. The urine and kidney function testswere normal and his blood-urea was 36 mg. per 100 c.cm.’The Wassermann reaction was negative. X ray examina-tion showed an enlarged heart. The electrocardiogramrevealed well-marked Q deflections, with inversion of the’T waves in lead III and low T waves in lead II. Lead IVwas normal. The findings suggested an old coronarythrombosis of T type.
Cardio-omentopexy was carried out on March 12th.Owing to a very large amount of pericardial fat thephrenic nerve was not seen, but it was crushed successfully- and a large fat omental graft was obtained. There wereinto pericardial adhesions. Aleuronat was used, and the
graft was not sutured to the heart but only to the peri-cardium. The blood pressure three hours after operationwas 130 mm. systolic and 88 diastolic. He developed amild purulent bronchitis. Pyrexia lasted for a fortnight,due partly to a quinsy which arose during the secondweek. X ray examination on the fourth day suggesteda small pericardial effusion. Serial electrocardiogramsshowed that the T waves became inverted in leads I andII and subsequently recovered. He was allowed upat the end of four weeks and was discharged home onApril 17th, his blood pressure being 155 mm. systolic and110 diastolic.He is now symptom-free and has had no angina since
the operation. He has moved into a larger house and isdriving a car again.
CASE 10
A shipping messenger, aged 41, was admitted to LambethHospital from Dr. A. W. Holthusen of Westcliff on
April 10th, 1937, complaining of attacks of angina sinceJuly, 1935. The pain "gripped him like a vice " andradiated down both arms. It was brought on by exertion,and had begun, with increasing frequency, to awaken himat night. He could walk no further than 100 yards andneeded 48 nitroglycerin tablets a week. He had had noprevious illnesses. His father had suffered from anginabut had had no attacks subsequent to a severe attack ofprobably coronary thrombosis on May 20th, 1933.
Physical examination showed a big man of rather flabbymusculature. His tongue was coated. The heart was notenlarged and there were no murmurs. The aortic secondsound was accentuated. The radial and brachial arterieswere somewhat tortuous and the blood pressure was184 mm. systolic and 110 diastolic. Nothing abnormalwas found in the chest, abdomen, and central nervoussystem. There was no oedema. The urine and kidneyfunction tests were normal. The blood-urea was 44 mg.per 100 c.cm. The Wassermann reaction was negative.X ray examination showed heavy hilar shadows and anincrease of the heart shadow to the right. The electro-
cardiogram was of large amplitude and showed notchedQ deflections in lead III. The T waves were low in lead I,flat in lead II, and diphasic in lead III, and there wasdepression of the S-T interval in leads I and II.
Cardio-omentopexy was performed on April 16th. Therewere some pleural adhesions. The heart was large, thepericardium tense but free, and there was a well-markedinferior sternopericardial ligament. A considerableamount of aleuronat was inserted, and the graft wassutured to the pericardium but not to the heart. Theblood pressure at the end of operation was 112 mm.
systolic and 70 diastolic. During the night the pulse-raterose to 144 and the systolic blood pressure the next morn-ing was only 68. Febrile reaction lasted over a week andleucocytosis reached 25,600 per c.mm. A soft pericardialrub was heard on the third day. On the sixth day hisgeneral condition and the physical signs suggested a lefthsemothorax, and this was confirmed by paracentesis andX ray examination. Convalescence was slow. He wasallowed up at the end of six weeks and was dischargedhome on May 29th. The electrocardiogram during thefirst week showed marked depression of the S-T interval inlead I and elevation in lead III.
Fourteen weeks after operation he looked well but wasgetting mild anginal attacks both on exertion and at rest.The heart sounds were tic-tac and a definite galloprhythm was present. The blood pressure was 168 mm.systolic and 100 diastolic. A month later the galloprhythm had disappeared but the heart sounds were stilltic-tac. He returned to light work on Sept. 30th, five anda half months after operation. He is now getting noserious pain and can climb the 72 stairs to his office without pain or distress. The heart sounds are of good qualityand the blood pressure 155 mm. systolic and 105 diastolic.The left diaphragm still shows paradoxical movement.
CASE 11 I
A tool-maker, aged 56, was admitted to Lambeth Hos.pital from Dr. F. B. Mallinson on Feb. 20th, 1937, with ahistory of angina pectoris for four years. Attacks werebecoming more frequent and might stop him three or
8 DR. DANIEL DAVIES AND OTHERS : SURGICAL TREATMENT OF ANGINA PECTORIS
four times during his twenty minutes’ walk to the station.He had had pleurisy twenty years ago and renal colic threeyears later, when he passed three small stones. He hadbeen a non-smoker since the age of 19 and was a totalabstainer. There was no family history of angina.On examination he appeared a well-nourished, grey-
haired man. The apex-beat was in the 5th intercostalspace, 4i in. out, and the cardiac impulse was heaving.The aortic second sound was thin and there was a softsystolic murmur at the apex. The arteries were notthickened and the blood pressure was 140 mm. systolicand 70 diastolic. Nothing abnormal was found in the chestand abdomen. The ankle-jerks were not obtained. Therewas no cedema, the urine and kidney function tests werenormal, and the blood-urea 32 mg. per 100 c.cm. TheWassermann reaction was negative. X ray examinationshowed very heavy hilar shadows and moderate enlarge-ment of the heart. The electrocardiogram showed leftaxis-deviation, with notching of the S deflections in lead III.The T waves were inverted in lead I (in June, 1935, theywere known to have been upright).He was discharged home for domestic reasons on
Feb. 28th and was readmitted on April 20th. He had been
working hard without severe pain, but the exertion of thejourney (carrying a light suitcase half a mile) brought himto a standstill with quite a severe attack. The electro-
cardiogram showed small R and notched S deflections inlead IV.
Cardio-pneumonopexy was carried out on April 23rd,omentopexy being prevented by numerous fine adhesionsbetween lung and mediastinum. The phrenic nerve wascrushed. The pericardium was not tense, the heart free,slightly enlarged, and yellowish in colour. The lower
part of the left upper lobe and the upper .part of thelower lobe were sutured to the cut edge of the pericardium,after insertion of aleuronat. The blood pressure at theend of operation was 125 mm. systolic and 75 diastolic.Recovery was uneventful, with moderate pyrexia andleucocytosis. He was allowed up at the end of four weeksand was discharged home on June 9th, having had nofurther attacks of angina. His blood pressure was 144 mm.systolic and 84 diastolic. The electrocardiogram had shownincreasing inversion of the T waves in leads I and II.He improved at first at home and only had one attack
during June, but by the end of August he was complainingof attacks as frequent as before operation and exactlysimilar, except that instead of stopping he could get rid ofthe pain by increasing his pace. He was readmitted andspontaneous pneumothorax was excluded by X rayexamination. The electrocardiogram showed considerableincrease of voltage, with recovery of the T waves exceptin lead I. The S deflections in lead IV still showed
notching. He now reports that he is hard at work, butstill unable to walk far without anginal pain.
CASE 13
A printer, aged 43, was admitted to Lambeth Hospitalfrom Dr. G. A. Shepherd on April 13th, 1937, with the.story that he had collapsed unconscious in his office onJan. 21st. For a week previously he had complained ofpain behind the breast-bone and two days before he hadbeen awakened by an attack of palpitation which lastedfour hours and frightened him considerably. He wastreated in bed for a week and then sent to the seaside,where he complained of pain in the chest on exertion.Nearly a month after the attack he was seen by a cardio-logist, who diagnosed it as coronary thrombosis andadvised four weeks in a nursing-home at complete rest,followed by four weeks’ restful holiday. During this
period his weight was reduced from 15 st. 6 lb. to 13 st. 5 lb.,and he complained of occasional attacks of pain. His
previous health had always been good and there was nohistory of angina in the family.
’
On examination he was well nourished and appearedapprehensive and highly strung. The heart was not
enlarged, the sounds were normal, and there were nomurmurs. The arteries were not thickened and the bloodpressure was 144 mm. systolic and 90 diastolic (comparedwith 130 mm. systolic and 90 diastolic in February, 1937).The chest moved rather poorly but was otherwise normal,and nothing abnormal was found in the abdomen. The
tendon reflexes were exaggerated. The urine and kidneyfunction tests were normal and the blood-urea was 24 mg.per 100 c.cm. The Wassermann reaction was negative.X ray examination showed very slight enlargement ofthe heart. The electrocardiogram showed well-markedQ deflections, with inversion of the T waves in lead IIIand low T waves in lead II. The S-T interval was risingin lead I and raised and falling in lead III. Lead IVwas normal. The findings were compatible with a healingcardiac infarction of T type. He was treated for a
fortnight before operation with a balanced diet, breathingexercises, and a sedative mixture.
Cardio-omentopexy was performed on May 7th. The
phrenic nerve was crushed and a good fatty graft obtained.The heart was large, the pericardium not tense and freeof adhesions, and the myocardium fatty and greyish-yellow in colour. Aleuronat was used and the graft suturedto the pericardium only. The blood pressure at the endof operation was 110 mm. systolic and 68 diastolic.Recovery was uneventful. Pyrexia lasted for fourteen
days and leucocytosis reached 21,200 per c.mm. Hewas allowed up at the end of four weeks and was dis.charged home on June 19th, the blood pressure being120 mm. systolic and 88 diastolic. The electrocardiogramunderwent no material change.For the first three months after discharge he complained
of some breathlessness on exertion, and had four attacksof mild retrosternal pain, and on examination his heartsounds were tic-tac. He is now free of symptoms andback at work, but still taking life rather more easily thanhe need. His heart sounds are normal and the bloodpressure 130 mm. systolic and 94 diastolic. The left
diaphragm has recovered its tone and movement. In the
electrocardiogram Q waves and inversion of the T wavesare still present in lead III, but the S-T interval is nownormal in leads I and III.
CASE 14
A french-polisher, aged 56, was admitted to the LondonJewish Hospital on April 9th, 1937, with a three months’history of angina pectoris. The first attack had occurredon walking, and at the time of admission they were comingon every three or four hours. The pain was very severebut was relieved by three nitroglycerin tablets. In
hospital the attacks became fewer and milder. He wastransferred to Lambeth Hospital on May 14th. He gavea history of influenzal pneumonia in 1918, broncho-pneumonia six or seven years ago, and winter bronchitisfor many years. There was no history of angina or othercardiovascular disease in his family.
Physical examination showed a well-nourished, freckledman, 5 ft. 5 in. in height. He was confined to bed but wasable to wash himself. Attacks were far less frequent andpain was now relieved by half a tablet of nitroglycerin.The apex-beat was in the 5th intercostal space, 4 in. fromthe midline. The mitral first sound was accentuatedand the aortic second sound thin. There were no murmurs.Auricular fibrillation was present, the ventricular rate being100 per min. There was no arterio-sclerosis and the bloodpressure was 130 mm. systolic and 80 diastolic. The chestmoved poorly but the lungs were normal. The abdomenwas soft and rotund and the central nervous systemnormal. There was no oedema. The urine contained a.
trace of albumin. The blood-urea was 28 mg. per 100 c.cm.and the kidney function tests were satisfactory. The bloodshowed polycythaemia and gave a negative Wassermannreaction. X ray examination showed a large triangularheart shadow. The electrocardiogram showed auricularfibrillation, left axis-deviation, and notching of the Q R Scomplexes. The main deflection in lead IV was negative-and notched. He was treated with Luminal and a
venesection of one pint.Thoracotomy was performed on May 28th. The pulse-
rate rose to 160 as soon as the chest was opened, soaleuronat was inserted into the pericardium and the
operation terminated. The pericardium was not tense..The heart was greyish-yellow in colour and free ofadhesions.
Recovery from the actual operation was fairly uneventful.He was afebrile for a week, and then ran a mild irregulartemperature for the next month, probably due to a small
9’DR. DANIEL DAVIES AND OTHERS : SURGICAL TREATMENT OF ANGINA PECTORIS
pleural effusion which developed at the left base. Leuco-
cytosis reached 14,400 per c.mm. on the third day. Onthe ninth day his mental state became slightly confusedand never quite regained normality afterwards. ByJuly 5th, five and a half weeks after operation, he wassitting up in the evenings and able to take a few stepsround the room. He had had no further attacks of angina.Five days later he became suddenly blue and dyspnoeicand mentally more depressed. Severe pleuritic paindeveloped on the right side, the sputum became blood-stained, and signs of pulmonary infarction were found atthe right base. His condition rapidly deteriorated, throm-bosis of the right femoral vein occurred on July 19th,and he died the following day.
There was no post-mortem examination. -
CASE 15
A widow, aged 65, was transferred to Lambeth Hospital:on April 9th, 1937, from Lewisham Hospital (L.C.C.),where she had been admitted on July 28th, 1936, for acoronary thrombosis of T type occurring that day.Before the attack she had complained of breathlessness onexertion for six years and for five years attacks of pre-cordial pain brought on by exertion as trivial as sewing.Since the occlusion she had remained confined to bedand had complained of a persistent feeling of constrictionround the heart, with exacerbations of pain needingmorphia. She gave a history of several pelvic operations;and Mr. Cecil Joll had removed a goitre 20 years ago.She had had winter bronchitis of late years and was
subject to laryngitis. Her father had dropped dead ofheart trouble.
Physical examination showed an obese woman, confinedto bed and becoming easily dyspnoeic on slight exertion.The heart showed accentuation of the first sound and asystolic murmur audible at the apex and in the aortic area.The blood pressure was 154 mm. systolic and 90 diastolic.There were rales at the right base. The abdomen wasnormal. She complained of paraestnesiae in the arms, andthere was diminished sensibility to pinprick and cotton-wool. The urine and kidney function tests were normaland the blood-urea was 28 mg. per 100 c.cm. TheWassermann reaction was negative. X ray examinationshowed enlargement of the cardiac shadow to the right,? aneurysmal. The electrocardiogram showed left axis-deviation. The T waves were still inverted in lead IIIbut the S-T interval was now normal.A month after admission she had an attack of severe
constricting pain round the heart and lost consciousnessfor about two minutes. Her pulse and colour were verypoor at the time but she recovered well. Attempts weremade to activate her but even the exertion of getting outof bed brought on an attack of pain.
Cardio-omentopexy was performed on June 4th. Thephrenic nerve was crushed and a fatty omental grafteasily obtained. The inferior sternopericardial ligamentwas well marked. The pericardium was fatty and rathertense over a slightly enlarged heart. The heart wasfree and showed no evidence of infarction. The graftwas sutured to the heart without aleuronat. The pulse-rate at the end of operation was 80 and the blood pressure105 mm. systolic and 68 diastolic. She developed apainful non-productive cough with much bronchial spasm,,and dyspnoea and cyanosis on movement, but no signs ofconsolidation were found. The blood pressure had returnedto its pre-operative level within a week. Dyspnaea onexertion persisted for about a month. The electro-cardiogram showed flattening of the T waves in leads I andII on the tenth day but recovery to normal in three weeks.Activation was begun seven weeks after operation and-she sat out of bed at the end of two months for the firsttime for over a year. She still complained of an occasionalfeeling of heaviness across the chest but no anginal attacks.She was transferred to St. Benedict’s Hospital forconvalescence on Oct. 22nd, having lost 1 st. by dieting.
She now reports that she is up and about the ward threeor four hours a day without symptoms.
CASE 17
A traveller, aged 65, was admitted to Lambeth Hospitalon June 29th, 1937, with a history of angina pectoris for a
year. Attacks had become so frequent, even occurringat rest, that in January, 1937, he had been admitted tohospital for treatment by paravertebral alcohol nerve-block. He had had no pain since, but was now complainingof increasing breathlessness on exertion and was unableeven to shave himself. There was no history of previousillness and no family history of angina.On examination he appeared a florid, grey-haired man.
The heart was not enlarged clinically, the sounds wererather toneless, and there were no murmurs. Moderatearterio-sclerosis was present and the blood pressure was132 mm. systolic and 88 diastolic. There were rales atboth bases. The vital capacity was 1900 c.cm. and thechest expansion 1 in. The liver was just palpable but nottender. The knee-jerks were not obtained. The urinecontained a trace of albumin. The blood-urea was 40 mg.per 100 c.cm. and the urea-concentration test 2-1 per cent.and 2-6 per cent. The Wassermann reaction was negative.X ray examination showed enlargement of the heart. The
electrocardiogram showed left axis-deviation and notchingof the Q R S complexes. The T waves were inverted inlead I and low in lead II. The main deflection in lead IVwas negative.
Cardio-omentopexy was performed on July 2nd. The
phrenic nerve was crushed but the diaphragm did notrise so <high or so dramatically as usual. The pericardiumwas tense but free of adhesions. Aleuronat only wasused for application of the graft, and the inferior sterno-pericardial ligament and lung fell nicely into apposition.The latter was unusually large, voluminous, and tough.The pulse-rate at the end of operation was 96 and theblood pressure 72 mm. systolic and 52 diastolic.
His condition was satisfactory until the fourth day,when signs of consolidation of the left lower lobe developed.On the seventh day a slight purulent discharge beganfrom the sternal end of the wound ; this proved ultimatelyto be due to necrosis of the 6th costal cartilage. The
pneumonia ran a satisfactory course until July 20th, whenhe became lethargic and on examination showed a drytongue, pulse less good, consolidated left lower lobe,enlarged and tender liver, slight oedema of the ankles andlumbar region, and much albuminuria. The bloodpressure was 114 mm. systolic and 78 diastolic. Theblood-urea was 68 mg. per 100 c.cm. In four days alloedema had disappeared but he remained drowsy. Two
days later an empyema burst through the outer end of hiswound and his mental condition improved at once. A
haemolytic streptococcus was isolated from the pus and5 c.cm. of Prontosil Soluble was injected on two occasionsinto the empyema cavity. He seemed to be improvingslowly, but necrosis of the costal cartilage was progressiveand on August 22nd his pulse was noted for the first timeas being less good. He died suddenly in his sleep threedays later, 7t weeks after operation.At pos<-t7KM’<etM examination the operation wound was
found to have healed except for two large sinuses ; one
at the sternal end exposed the 6th costal cartilage, whichwas ununited to its rib and in a condition of necrosis ;the other led backwards into the axilla to a sinus enteringthe pleural cavity. The heart was rather small and themyocardium soft and fibrotic. Both coronaries were
calcined for the first 2 in. of their course, and their luminawere almost completely obliterated. There was one smallsuperficial adhesion high up over the left ventricle anda dense tubular adhesion to the anterior aspect of theapex. This corresponded outside the pericardium to adensely adherent mass consisting of fatty inferior sterno-pericardial ligament, portion of left lung, left dome ofdiaphragm, and thoracic end of the graft. There was asmall empyema cavity, empty of pus, over the lower halfof the left lower lobe. The upper lobe of the left lung wasnormal. Its lower lobe was collapsed and the cut surfaceshowed thickened and dilated bronchioles protruding fromthe retracted lung parenchyma. The right lung showedbasal congestion and oedema. The aorta showed diffuseearly atheroma. In the abdomen the omental graftpassed through the left leaf of the diaphragm near itslateral attachment. The liver was fatty and the spleentoxic and diffluent. The kidneys were rather large andshowed congestion on section. The capsule stripped easily,leaving a smooth surface. On histological examinationthe myocardium showed extensive fibrosis and areas of
10 DR. DANIEL DAVIES AND OTHERS : SURGICAL TREATMENT OF ANGINA PECTORIS
recent infarction. There were many patent blood-vessels inthe graft lying over the epicardium, and there was alsoa very vascular subepicardial zone corresponding to it,as seen in Case 2. The specimen is receiving furtherhistological study.
CASE 18
A housewife, aged 62, was admitted to Lambeth Hospitalon April 23rd, 1937, with a six years’ history of anginapectoris. During the last year her activity had been somuch curtailed that she had been unable to go shopping.Pain had occasionally occurred in bed. She was also veryshort of breath, had a bad cough, and slept badly. Shewas in bed for three months with rheumatic fever at theage of 18. There was no family history of angina. Shecontinued to have attacks of angina while in hospital, andafter a severe attack on June 30th she was referred to theclinic.
Physical examination showed a rather obese and floridwoman. There was gross oral sepsis. The heart was
enlarged, the sounds were soft and spaced with a well-marked gallop rhythm, and there was a very soft mitralsystolic murmur. The arteries were not thickened andthe blood pressure was 186 mm. systolic and 106 diastolic.There were rales at both bases ; the vital capacitywas 1500 c.cm. and the chest expansion t in. Theabdomen was normal and the central nervous systemalso except for small irregular sluggish pupils. Therewas no oedema. The urine and kidney function testswere normal and the blood-urea 26 mg. per 100 c.cm.
The Wassermann reaction was"negative. X ray examina-tion showed an enlarged heart. The electrocardiogramshowed left axis-deviation and inversion of the T wavesin lead I. The duration of Q R S was 0.12 sec.
All her teeth were extracted. When re-examinedbefore operation, gallop rhythm was only just discernible,but the heart sounds were still tic-tac. There were veryfew basal rales and the blood pressure was 164 mm.systolic and 90 diastolic.
Cardio-omentopexy was performed on July 2nd. Thephrenic nerve was crushed and a good graft obtained.The lung was emphysematous and a bulla could be seenposteriorly. The pericardium was tense and containedexcess of fluid. The surface of the heart showed a palearea. Aleuronat was applied and the graft sutured to theedge of the pericardium. A well-marked inferior sterno-pericardial ligament and the lung fell nicely into apposition.The pulse-rate at the end of operation was 110 and theblood pressure 104 mm. systolic and 66 diastolic.Her immediate progress was good. She developed
purulent bronchitis and a urinary infection, both of whichsettled down. Tachycardia and leucocytosis however,persisted for no obvious cause, and three and a half weeksafter operation she had an anginal attack lasting fifteenminutes. Her condition then slowly improved and byAugust 9th she had been up twice without ill effects.The following day she had two further attacks and wasconfined to bed again. Eight weeks after operation shewas still confined to bed and was getting frequent attacksof pain, relieved by nitroglycerin. On examination theheart was not enlarged. There was tachycardia but nogallop rhythm. Very slight pitting cedema was presentover the tibiae. The blood pressure was 150 mm. systolicand 84 diastolic. She died suddenly on Sept. 6th, twomonths after operation.At post-mortem examination the wound was found soundly
healed. The left lung and the inferior sternopericardialligament were adherent to the graft, which was itselfadherent to the heart. There was complete adhesionof the pericardium, and on separation of part of it severalbleeding points could be seen on the surface of the heart.The heart showed hypertrophy of the left ventricle, withdiffuse fibrotic changes in the myocardium. The coronarytree showed diffuse sclerosis and atheroma, but detailedexamination of its ramifications was not carried out as thespecimen is being preserved for further histological studyof the adhesions, which initial examination shows to behighly vascular. The lungs were normal. The abdominalviscera were not abnormal and the graft could be seenpassing through the diaphragm at its normal site. Thecolon was not kinked.
CASE 19
An engineer, aged 55, was admitted to Lambeth Hospitalfrom Dr. Blair Macaulay of Liverpool on July 26th,1937, complaining of breathlessness on exertion of gradualonset, 3i years ago, when working long hours under badconditions on the Mersey Tunnel. Soon afterwards hehad begun to get attacks of pain across the chest onexertion. At the time of admission he could not walkmore than twenty or thirty yards without inducing anattack. His previous history was negative except for aherniotomy ten years ago, and there was no family historyof angina.
Physical examination showed a lean but well-nourishedman of florid complexion. The tongue was moist and clean,but the gums round his six remaining teeth showedpyorrhoea. The heart was not enlarged, the sounds wereonly just audible, and there were no murmurs. The radialand brachial arteries were moderately thickened and theblood pressure was 100 mm. systolic and 70 diastolic.There were a few persistent rales at the right base and aconstant cough was noticeable. The chest expansion was1 in. Nothing abnormal was found in the abdomen.The urine contained a trace of albumin. The blood-ureawas 44 mg. per 100 c.cm. and the urea-concentrationtest was normal. The Wassermann reaction was negative.X ray examination showed a normal heart shadow. The
electrocardiogram showed a low voltage, the Q R Scomplexes measuring 1 mm. in lead I. The T waves wereupright in all leads but low in lead I.He was treated with breathing exercises and a stimulat-
ing expectorant mixture, and his remaining teeth wereextracted. His cough and sputum persisted, however, andit was decided that he was only fit for pericardiotomy viaLarrey’s angle. This operation was advised in the hopethat he might improve sufficiently to allow cardio-omentopexy to be performed at a later date. His vital
capacity before operation was 3150 c.cm.Pericardiotomy via Larrey’s angle was performed on
August 28th. The heart was greyish-yellow in colour.In spite of the minor nature of the operation he developedpurulent bronchitis with mild pyrexia but no leucocytosis.He was allowed up for the first time two and a half weeksafter operation and was discharged home for personalreasons on Sept 23rd, his blood pressure being only 96 mm.systolic and 66 diastolic. He was able to walk roundthe grounds and up one flight of stairs without pain orbreathlessness.
’
His improvement was short-lived and he now reportsthat his condition is as bad as before the operation.To sum up, of these fifteen cases of angina sub-
mitted to operation we record five deaths : one ofuraemia in a man aged 72, three months after opera-tion ; the second at operation through rupture of afriable ventricle ; the third of pulmonary infarctiontwo months afterwards ; the fourth suddenly inthe second month, following a stormy convalescencecomplicated by pneumonia, empyema, and necrosisof a costal cartilage ; and the last suddenly for noapparent cause, again two months after operation.On the other hand, of the ten who lived we have know-ledge that eight have eventually enjoyed freedom fromangina, and of the eight men seven are back atwork.
(To be concluded)
MENTAL AFTER-CARE ASSOCIATION.—The object ofthis association is to provide some form of assistance,including homes for convalescence, for the poor treatedin public mental hospitals to bridge over the diffi-cult period intervening between recovery and returnto normal life. Later some are helped to find suitableemployment. This year nearly 4000 people have beenbefriended by the association. It also assists authoritieswho are adopting the boarding-out system for chronic
patients. An earnest appeal for funds to carry on andextend this work is being made. Contributions should besent to Miss E. D. Vickers, 354, Grand Buildings, London,W.C.2.
11DR. JONES : OVER-ACTIVITY OF THE POSTERIOR PITUITARY
A NEW SYNDROME APPARENTLY DUE TO
OVER-ACTIVITY OF THE POSTERIOR
PITUITARY
BY E. IDRIS JONES, M.D., M.Sc., M.R.C.P. Lond.MEDICAL REGISTRAR, KING’S COLLEGE HOSPITAL, LONDON ;
LECTURER IN BIOLOGY, ST. MARY’S HOSPITAL
A PATIENT presenting the combination of hyper-tension, hyperchromic anaemia., achlorhydria, andabnormal carbohydrate tolerance has been investi-
gated for the past eight months and, as this syndromehas not been previously reported, a preliminaryaccount is given here.
CASE-HISTORY
A. B., aged 26, an insurance broker, was first seen onMarch 7th, 1937, complaining of " not feeling fitand of nose-bleeding.He had had intermittent epistaxis for a week in March,
1937, and since then had had lethargy, discomfort inthe lumbar region, and occasional diffuse headaches.There was undue dyspnoea on exertion and he had aslight cough. There were no urinary or gastro-intestinalsymptoms but he had occasional " thumpings of theheart." He smoked 15-20 cigarettes daily. His weightwas stationary and he had a good appetite with a preferencefor fatty foods and an avoidance of salt at all times. Thebowels acted regularly. Previously he had always beenwell; he could not date the definite onset of the symptomsapart from the epistaxis. His father died of " angina
"
at 55 ; his mother and one brother were alive and well.
TABLE I-SUMMARY OF BLOOD COUNTS
discont. = discontinued.
Examination.-The patient is a lean athletic man ofsallow complexion with hair thinning in the frontal regionand the vertex. Height, 5 ft. 10 in. ; weight, 155 lb. ;tongue normal; teeth good. Pulse 72, regular and of goodtension, arteries not obviously thickened; apex-beat4 in. from the midline in the fifth intercostal space ;no cardiac enlargement to the right of the sternum ;heart sounds normal apart from accentuation of theaortic second sound ; blood pressure in both arms 190/110,and in the legs 200/110. Lungs: nothing abnormaldiscovered. Abdomen : ? tip of spleen just palpable.Nervous system : reflexes all present and brisk ; sensationnormal ; pupils dilated, reacting briskly to light andaccommodation. Fundi : veins full, arteries some-
what narrowed; no haemorrhages or exudate. Urine :sp.g. 1022, pH 5-7 ; ; no albumin, sugar, acetone, or
blood ; trace of urobilinogen; oxalate crystals -/---E- ;chlorides ----E--
SPECIAL INVESTIGATIONS
Radiography showed clear lung fields and a heart-
lung ratio within normal limits ; the pituitary fossa wasnormal, almost roofed over, and the sinuses were clear.
Capillary resistance (tourniquet test) : strongly positive.Blood counts are summarised in Table I.
Gastric residuum (six hours after last meal).-May 6th,1937 : 8 c.cm. of opalescent- fluid removed with difficulty ;no free HC1; total acids (combined acid) equivalent to1-5 c.cm. of N/10 NaOH or 0-0054 per cent. HCl. After0-25 mg. histamine subcutaneously only 5 c.cm. of gastricjuice could be obtained twenty minutes later ; no free
HC1; total acids equivalent to 2-3 c.cm. of N/10 NaOHor 0-0083 per cent. HC1. The two samples were similarin appearance and there was a considerable quantity ofmucus.
TABLE II-BLOOD-SUGAR CURVE OF THE PATIENT INMAY, 1937
11’cces.-Formed, brown, no abnormal amount of mucus,no blood ; large numbers of soap flakes present and a fewfat droplets. Fat estimation on dried fmce8 (May 23rd) :total fat 31 per cent., total fatty acids 21 per cent., andneutral (unsplit) fats 10 per cent.Renal function.-Early morning fasting specimen:
sp.g. 1022, volume 150 c.cm., urea 3 g. per 100 c.cm.Then 15 g. of urea were taken in 100 c.cm. of water, and1 hr. 50 min. later sp.g. was 1020, volume 150 c.cm.,and urea 3 g. per 100 c.cm. ; 3 hr. 30 min. later sp.g. was1022, volume 113 c.cm., and urea 2-85 g. per 100 c.cm.(The patient found it impossible to pass urine at hourlyintervals after the dose of urea.) Water-elimination test :after ingestion of 20 oz. water, 16.5 oz. of urine was passedwithin three hours. Blood-urea : 86 mg. per 100 c.cm.
Blood-sugar curves.-See Tables II and III. (Method ofHagedorn and Jensen on capillary blood.)
Further tests on August 8th.-Van den Bergh : directreaction negative. Blood chlorides : 612 mg. per 100 c.cm.
(Van Slyke method). Serum calcium : 8-8 mg. per 100 c.cm.(Clark and Collip).
COMMENT AND DISCUSSION
The combination of a hyperchromic anaemia, andhypertension in a patient aged 26 was at first thoughtfortuitous ; but the fact that Dodds, Noble, andothers (1935a and b) had produced a hyperchromicanaemia in animals by means,of posterior pituitaryextract made one consider the possibility of hyper-function of the posterior pituitary. Cutting, Dodds,and others in 1937 also produced achlorhydria withthe extract, and the achlorhydria of this patient,together with his abnormal carbohydrate tolerance,strengthened this possibility, on which the followingdiscussion is based.The blood picture (Table I) was at first that of a
hyperchromic anaemia. After administration of liverthe blood count returned rapidly to normal, but ondiscontinuing liver the red cell count fell again. Itwas restored to normal when liver was again given,and though liver therapy was entirely discontinuedafter a month the blood picture has remained approxi-mately normal since. Associated with this anaemiawas a histamine-refractory achlorhydria. The vanden Bergh reaction was unfortunately not done atthe time when the patient was anemic.
A 2
